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According to the Guinness Book of World Records 2001, gum (periodontal) disease is the most commonly occurring disease in humans. Severe gum disease (periodontitis) is characterized by the bacteria-induced inflammatory destruction of tooth-supporting tissues and alveolar bone. Periodontitis remains the most common cause of tooth loss in adults worldwide. Emerging scientific evidence shows that the effects of gum disease are not limited to the mouth and it is also associated with cardiovascular disease, stroke, diabetes mellitus, adverse pregnancy outcomes, and lung infections. It is believed that gum disease is one of the most important global oral health burdens.

PI's previous studies funded by RGC indicate that gum tissues serve not only as a physical barrier protecting teeth, but also more dynamically as a biological barrier keeping harmful oral microbes under control by producing various forms of ‘natural antibiotics' (e.g. human ß-defensins, hBDs) and other molecules related to the natural immunity of the gums. An ongoing pioneering study, funded by the National Institutes of Health, US, which the PI is currently performing in collaboration with colleagues from the US and UK, will enrich this story.


Severe gum disease


Gum disease controlled after treatment

Porphyromonas gingivalis lipopolysaccharide (LPS) is a crucial virulence factor strongly involved in the development of gum disease. It displays a significant amount of lipid A structural heterogeneity. Little is known on how the different isoforms of P. gingivalis LPS could differentially affect host innate immune responses in human gingival epithelia. The present study compares the modulatory effects of different isoforms of P. gingivalis LPS on the expression of hBDs in the reconstituted human gingival epithelia (RHGE), and examines the involvements of a panel of pattern recognition receptors in the modulatory effects concerned.

P. gingivalis
LPS
1435/1449 and LPS1690 were isolated from P. gingivalis ATCC 33277 and further highly purified. The RHGE were incubated with the two isoforms of P. gingivalis LPS in both concentration- and timedependent assays. For blocking assay, RHGE were pre-incubated for 1 h with anti-human.TLR2/4 and CD14 monoclonal antibodies. RHGE were then harvested for protein assay by immunohistochemistry and ELISA, and for detection of the target mRNAs by RT-PCR/realtime PCR, respectively.

The isoform of Porphyromonas gingivalis LPS toxin (LPS1435/1449) was shown to greatly affect the gene expression and protein production of hBD-2, through a newly discovered TLR2/4-dependent mechanism. This outcome may significantly weaken the biological barrier of the gums and could be related to the pathogenesis of gum disease.

The current findings are helping to further our understanding of how pathogenic oral bacteria affect gum cells. The full identification of the biological mechanisms involved is an approach that holds great promise in the development of novel means of preventing and treating gum disease. The benefits will be both better oral health and general health.


Prof. Li-jian Jin
Faculty of Dentistry
The University of Hong Kong
ljjin@hkucc.hku.hk

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